Neurogenesis (birth of neurons) is the process by which neurons are created(Gage,2003;Mohapel,Leanza,Kokaia&Lindvall,2006;Prickaerts,Koopmans,Blockland&Scheepens,2004). Most active during pre-natal development, neurogenesis is responsible for populating the growing brain.

The discovery of adult neurogensis raises new possibilities in the treatment of neurological disorders and brain and spinal cord injuries (Van Praag,Zhao,&Gage,2004).

Many of these newborn cells die shortly after their birth, but a number of them become functionally integrated into the surrounding brain tissue.

Adult neurogenesis has been the subject of an historical dogma, and only recently has its existence been largely accepted by the scientific community. While it is reasonably well-accepted that hippocampal neurogenesis does occur (see for example Eriksson et al., 1998; Gould et al., 1999a), some authors (particularly Elizabeth Gould) have suggested that adult neurogenesis may also occur in other areas including human neocortex (e.g., Gould et al., 1999b; Zhao et al., 2003). Others, including Rakic (2002), have questioned the scientific evidence of these findings; in the broad sense, they suggest that the new cells may be glia.

The function of adult neurogenesis is not certain [1] - although there is good evidence that hippocampal adult neurogenesis is important for learning and memory. This is perhaps unsurprising given what we know of the hippocampus and its role in learning and memory (several authors, including, for example, Rolls & Treves (1998) have postulated integrated theories for the role of hippocampus in learning and memory). Gould et al. (1999c) have demonstrated that the act of learning itself is associated with increased neuronal survival.

Malberg et al. (2000) [2] and Manev et al. (2001) [3] have linked neurogenesis to the beneficial actions of certain antidepressants, suggesting a connection between decreased hippocampal neurogenesis and depression. In a subsequent paper, Santarelli et al. (2003) demonstrated that the behavioural effects of antidepressants in rats did not occur when neurogenesis was prevented with x-irradiation techniques. Very recent papers have linked together learning and memory with depression, and have suggested that neurogenesis may promote neuroplasticity. For instance, Castren (2005) has proposed that our mood may be regulated, at a base level, by plasticity, and so chemistry; for instance, the effects of antidepressant treatment is only secondary to this.

Various other factors may increase or decrease rates of hippocampal neurogenesis. Even voluntary exercise (e.g., Bjornebekk, Mathe & Brene, 2005) seems to promote their survival and successful integration into the existing hippocampus. On the other hand, stimuli such as chronic stress can decrease their proliferation. The link between stress, depression, and the hippocampus is well-documented (e.g., Lee et al., 2002; Sheline et al., 1999).

Neural stem cells (NSCs) are the self-renewing, multipotent cells that generate the main phenotypes of the nervous system. In 1992, Reynolds and Weiss were the first to isolate neural progenitor and stem cells from the striatal tissue, including the subventricular zone – one of the neurogenic areas - of adult mice brain tissue (Reynolds & Weiss, 1992) [4]. Since then, neural progenitor and stem cells have been isolated from various areas of the adult brain, including non-neurogenic areas, such as the spinal cord, and from various species including human (Taupin & Gage, 2002) [5]. Epidermal growth factor (EGF) and fibroblast growth factor (FGF) are mitogens for neural progenitor and stem cells in vitro, though other factors synthesized by the neural progenitor and stem cells in culture are required for their growth (Taupin et al., 2000) [6]
. It is hypothesized that neurogenesis in the adult brain originates occurs from NSCs. The origin and identity of NSCs in the adult brain remain to be defined.